“Future refinement of case definitions may wish to focus on requiring a small set of core symptoms such as post-exertional malaise, neurocognitive symptoms and possibly unrefreshing sleep”. Jason et. al.
Background
There’s something right about doing a birthing a definition blog on Christmas. Disease definitions are about new beginnings – about clarity, about really zeroing in on a disorder so that researchers and drug manufacturers can be more effective. A good definition that works makes everything easier.
Make no doubt about it – after 20 years – a new research definition is coming
We’ve heard a lot recently from the P2P panel and earlier from the IOM project about finding or creating a definition for chronic fatigue syndrome (ME/CFS). Earlier this year fifty advocates and many in the ME/CFS signed a petition requesting the Dept. of Health and Human Services (DHHS) accept the Canadian Consensus Criteria at least in the short term as both the clinical and the research definitions for ME/CFS.
That idea was rejected as the federal government brought in outside researchers and in the case of the IOM panel, ME/CFS experts, to do their own analysis of the situation. Neither the AHRQ report nor the P2P draft report settled on a definition; instead the P2P report called for an international network to come to a consensus on a definition and then lay out a roadmap to refine and clarify it.
Make no doubt about it – the Fukuda definition that has ruled the roost for the past twenty years in ME/CFS research is on its way out. There’s too much momentum for change for a new definition not to occur. The big question is what it will be.
The Biggest Need – A Research Definition
In this blog we’re talking about a research definition – not a clinical one. Research definitions do not describe the disease – clinical definitions do. Usually short and concise, research definitions ensure that people with the core aspects of a particular disease – and only that disease – make their way into research studies.
Because research definitions are not in the ordinary sense representative they can look a little, well, odd
Unlike a clinical definition that seeks to include all types of patients in it, a research definition will exclude some people who have the disorder. It may not look particularly representative. It may not include some prominent symptoms and may include less prominent symptoms. The makeup of a symptom-based research definition will depend on not on the most recognizable symptoms, but what symptoms are unique to it relative to those found in other disorders.
The research definition is the greatest need and the IOM panel is not tackling that – perhaps for fear of opening a can of worms. But what if we’re already pretty close to a research definition – one that needs little modification? One that was derived not through a consensus approach –something the AHRQ panel specifically warned about – but using a statistically rigorous approach? What if the basic components of a new definition are sitting right under our noses? If Lenny Jason’s latest study is correct, we very well may be.
A Little History – A Little Mystery
Leonard Jason, M. Sunnquist, A. Brown, M. Evan et. al. 2014. V Examining case definition criteria for chronic fatigue syndrome and myalgic encephalomyelitis. Fatigue: Biomedicine, Health and Behavior. Vol 2, No. I, 40-56.
Jason has been comparing the different definitions for several years now and in the first part of his paper he went over the definitions and what his studies have found.
Holmes Definition (1988) – The first definition, the Holmes definition, required a person to have 8/11 symptoms. On the face of it, the definition with its sweeping symptom set (fever or chills, sore throat, lymph node pain, muscle weakness, muscle pain, post-exertional malaise, headaches of a new or different type, migratory arthralgia, neuropsychiatric complaints, sleep disturbance and sudden onset) looks quite good, but it was discarded when it was found that requiring 8 symptoms inadvertently selected out patients with high rates of psychiatric diagnoses.
Fukuda (1994) – the collapse of the Holmes definition lead to the Fukuda definition which required, along with life-altering fatigue, a patient have four of eight symptoms. By not requiring core symptoms such as post-exertionaly malaise, however, the Fukuda definition ran the risk of allowing people without core ME/CFS symptoms into ME/CFS research studies.
Canadian Consensus Criteria (CC) (2003) – created by physicians and researchers this definition focused on core symptom domains found in ME/CFS and required that patients experience post-exertional malaise plus seven core symptoms.
International Consensus Criteria ICC) (20 ) – an updated version of the CCC, the ICC again highlighted post-exertional malaise and required ME/CFS patients to have eight symptoms.
The consensus definitions look right and feel right but in the end they might not be right – for a research definition
A Little Mystery – Jason’s comparisons of people meeting the CCC and ICC and Fukuda criteria indicate that the CCC and ICC definitions do select out patients who have the core symptoms of ME/CFS (Fukuda does not). They also more accurately identify people who have ME/CFS, and they identify patients who are more severely ill than the Fukuda definition does.
Jason’s studies also indicate, however, that the CCC and ICC select out patients with significantly higher rates of psychiatric disorders than Fukuda does probably, because, like the Holmes definition of 1988, they require patients to have more symptoms.
It’s perhaps telling that Jason, our resident expert on definitions and characterizing symptoms did not participate in the creation of either the CCC or the ICC. The two definitions look good on paper and they provide superb characterizations of the illness, but the studies suggest they’re better off being used as clinical definitions for doctors than as research definitions.
Importantly, none of these definitions assess symptoms according to their frequency/severity – they simply require that a symptom be present – and that will end up making a big difference.
The Study
Appearing in the IACFS/ME’s “Fatigue: Biomedicine, Health and Behavior journal earlier this year, Lenny Jason’s study “Examining case definition criteria for chronic fatigue syndrome and myalgic encephalomyelitis” took a big step towards producing a statistically derived research definition for ME/CFS.
The study used data from over 300 participants in the SolveCFS BioBank and healthy controls. Each took the DePaul Symptom Questionnaire that had been developed specifically for ME/CFS by Jason at DePaul University. The questionnaire uses frequency (from 0=none to 4=all the time) and severity (from 0=not present to 4=very severe) measures to assess the importance of 54 symptoms. Someone, for instance, who infrequently has mild headaches will have a much lower score (n=2) than someone who often has severe headaches (n=8).
The symptoms in the questionnaire include everything from fatigue and extreme tiredness to pain to stiffness in the joints to sensitivity to noise to night sweats to alcohol intolerance to fever.
Study Aims
Since having healthy controls make it into ME/CFS research studies as patients is not a good thing, Jason first used the DePaul Questionnaire results to determine what percentage of ME/CFS patients and healthy controls met the Fukuda, Canadian and International Consensus Criteria for ME/CFS. First he assessed the definitions as they are – simply requiring that a symptom be present or not. Then he introduced severity into the equation by requiring that for a symptom to count it had to be present at least half the time and be of moderate severity.
He also used an algorithm that identified which symptoms best differentiated the ME/CFS patients from the healthy controls.
Results
The Fukuda Definition Goes Down – Hard….
All the consensus definitions – the Fukuda, CCC and ICC – misclassified significant percentages of healthy controls as having ME/CFS
The Fukuda definition has taken some blows over the years, but probably none greater than Jason’s finding that a third of the healthy controls meet the Fukuda criteria for CFS. The Fukuda definition’s criteria that anyone having 4/8 symptoms plus fatigue apparently didn’t prove much of a bar.
When Jason required that a symptom be moderately severe and present at least half the time to fulfill the Fukuda criteria, however, only 5% of the health controls were diagnosed with having ME/CFS.
Canadian Consensus Criteria (CCC) and International Consensus Criteria Take Their Hits
Before you laugh too much at the poor Fukuda definition, get this – the CCC and ICC fell into the same trap – albeit to a lesser degree. Twenty-one percent and 16% of the healthy controls meet the CCC or ICC criteria for ME/CFS if the symptoms in those definitions were simply required to be present.
If, however, the symptoms were required to be present at least half the time and be of moderate severity just 4% of the healthy controls met either criteria for having ME/CFS.
The moral of the story is that adding frequency and severity characteristics to a symptom-based definition is critical.
Jason also found that the four core symptoms that occurred with the highest prevalence in ME/CFS patients were fatigue, post-exertional malaise, neurocognitive problems and unrefreshing sleep. Pain, autonomic, immune and neuroendocrine symptoms were not as common. Muscle pain was moderately common in the ME/CFS patients but since it was fairly common in the healthy controls it would not be a good distinguishing factor.
The Perils of Consensus
It’s clear that the two consensus criteria (CCC,ICC) do pluck out more severely ill patients than Fukuda, but they fail on two aspects:
- significant percentages of healthy controls meet their criteria for ME/CFS
- ME/CFS patients that meet the criteria tend to have higher rates of psychiatric disorders.
It’s findings like this that explain why consensus definitions or findings are viewed with some skepticism. Consensus findings that appear on the face of it to make perfect sense, as the CCC and ICC do, don’t always work.
The Next Research Definition?
Heavy feelings (cement legs anyone?) after exertion was one of three core symptoms in ME/CFS
Creating a definition that incorporates frequency and severity into it and doesn’t require a lot of symptoms is clearly a priority. Jason’s data mining analysis indicated, however, that so long as you require that a symptom be present at least half the time and have moderate severity, just three symptoms are needed to correctly differentiate almost all the ME/CFS controls from the healthy controls.
Three symptoms below
- fatigue or extreme tiredness
- inability to focus on more than one thing at a time
- experiencing a dead or heavy feeling after starting to exercise
correctly identified 95% of ME/CFS patients and controls.
Fatigue, Cognition and Post-Exertional Malaise Highlighted
Note that the symptoms correspond with three of the four core symptom domains – fatigue, cognition and post-exertional malaise – Jason identified in this study. Symptoms from these domains are likely going to make up the next research definition for ME/CFS. Unrefreshing sleep might make it or it might not; apparently it’s on the cusp. Although pain is ‘moderately common’ in ME/CFS it’s not going to make it into the definition. Sensitivity issues are apparently not common enough to make into the core definition for ME/CFS but Jason suspects they will identify subsets. (He has a formula for identifying subsets as well.)
It’s interesting that fatigue, a common symptom, made the cut. This is presumably because while fatigue is common, more severe fatigue is not that common and fatigue that’s associated with problems in multitasking (problems focusing on more than one thing) and experiencing a heavy feeling after exercise is very uncommon in healthy people.
Some of the fatigue or exertion-based symptoms that didn’t make the cut include “next day soreness or fatigue after non-strenuous, everyday activities”, “being mentally tired after the slightest effort” and “minimum exercise makes you physically tired and feeling physically drained or sick after mild activity”.
It’s time for a more rigorous, statistically based approach to creating a research definition
Either these symptoms were too common in the healthy group or too uncommon in the ME/CFS group for them to differentiate the two groups. My guess is that heavy feelings after exercise are so common and so noticeable that that symptom easily made the cut despite (or maybe because of) the fact that it’s kind of odd. Who, after all, hasn’t experienced heavy legs after they over-do it?
New Era in Definition Creation
This large study of rigorously identified ME/CFS patients opens a new era in how to produce a definition. The well-loved consensus definitions played an important role in clarifying the key symptoms in ME’/CFS, but they are not appropriate as research definitions. Statistically determined definitions, on the other hand, will likely elicit trust from all the important stakeholders (drug companies, researchers, funders) in the medical world.
Next up Jason and company need to compare the symptoms found in ME/CFS with those in closely related disorders such as fibromyalgia and multiple sclerosis. Jason got an NIH grant to do this study. Hopefully with the P2P report calling for a new definition, he’ll get another grant to do the next one. That study is going to be interesting.
For ME/CFS: I think the feeling of intracranial pressure and inflammation is important as well. That seems to be very common.
I agree intracranial pressure is a big issue
Yes, it is very important. Perhaps this question wasn’t asked in the interviews for the research by Jason. After all, it has been proven that the brains of ME patients are quite inflamed.
Totally agree with Intracranial pressure, too
Definitely agree! It’s very unique to ME/CFS in my opinion…or a brain tumor. Ha. As a teen I had this sensation much worse than this flare at 22. At that time they did an MRI and it was clear. Then it was not known yet that I had ME/CFS. Cognitive dysfunction and lack of good short term memory/major mental fatigue are major hallmarks too.
Check out this blog – Pressure Building? Study Suggests Cerebral Spinal Fluid Pressure May Be Causing Problems in Chronic Fatigue Syndrome
http://www.cortjohnson.org/blog/2014/06/04/pressure-building-cerebral-spinal-fluid-chronic-fatigue-syndrome/
Thanks, yes, I remember that posting. I think a main point of the ME/CFS research is to remove the idiopathic adjective attached to the description of the intracranial pressure involved.
I am now 58 years old with CFS/ME. I remember thinking in high school that I might have a brain tumor. I always had a headache for a season and then it lifted. I’m beginning to think all of this is related.
Why aren’t they adding some biomarkers to help with a diagnosis like nk function and the 2day exercise test, I’m sure they could add more but I think just adding these two will give a cleaner diagnosis.
Hi Danny, they cannot add CPET to a definition because not everyone can do that safely. However it is a great tool for research.
I think we will see some blood or even brainscan markers added soon. Apparently not even NK cell testing is ready exactly at this moment (it should be widely available, as well as being validated, to be used in this way), but may be ready soon.
I agree with you, Danny. Those biomarkers are a very important part of defining this disease. Hope they get squeezed in there soon.
I think these two comments illuminate my feeling that trying to reduce the number of symptoms in defining any condition only leads to problems. If we know anything from all the discussions we have here- it’s how heterogeneous our symptoms are.
I agree that absolutely it must be determined the degree and severity of the symptom, but I know of no diseases where all patients have all of the given symptoms- there is always some variability.
In most diseases there is a core of symptoms and secondary symptoms that may or may not be present. There are other diseases like Sjogrens where the classic signs only show up after the secondary signs have been present for years, or don’t show up at all.
It seems to me that something like a reworking of the Fukuda with hindsight might not be such a bad thing?
Gregory, I think you are missing the point that this article is talking about research not clinical criteria. Research has been plagued by study populations being contaminated by normal and psychiatric subjects. We desperately need an era of research on true CFS populations. Patients having different CFS presentations may be excluded from such research studies but they will ultimately benefit form findings based on true CFS subjects.
So frustrating I did a VO2 max test and the result was so abnormal that the guy doing the test thought the machine was broken… His boss said no that is normal and diagnostic for someone with ME/CFS.
He said this research has been around since 2006!!! Ie it is not new. His words were a healthy person can’t burn carbs the way a person with ME/CFS does!!!!
That and the 2 day exercise test!!! Seems like there is a breakdown in communication between the medical researchers and the exercise physiologists.
Come on guys !!! PEM for me is the weirdest and clearest symptom the first sign I had that something was wrong!!!
🙂 I agree!!!
I think it’s cool to be thinking of new, data-based ways to sort this problem.
This way of diagnosing would have missed me when I was a new and mild patient. I probably developed PER in the first years but it was more concentrated on sore throat at that point than on heavy feeling in limbs. My fatigue was not severe at that point, either. While I realize clinical definition is meant to be different, it would be a shame to miss researching both groups, new and long-term, that the Lights seem to be finding. I think the symptoms may be in different sets.
I took the DePaul questionnaire, and while I do not remember specific questions, I do remember my overall impression which was that the questions were not good enough. They weren’t clear or comprehensive enough. Data from questionnaires is only as accurate and representative as the questions are pertinant and unambiguous. I was surprised because I think very highly of Lenny Jason. He knows this subject very well. I hope that in future studies, he/they work on clarifying the questions and making them very specific and unambiguous.
I firmly believe that the most critical issue in terms of learning useful information about M.E. is for severely ill patients to be the sole focus of upcoming research studies, rather than mostly or wholly ignored by researchers as they have been in most studies in the past. So I am happy to see severity being discussed as an important variable.
However, the idea that 16% of controls in any study would qualify for the ICC (which requires a lot of really specific symptoms plus a decrease to 50% or less activity compared to previous baseline) really redefines the meaning of the word “healthy,” doesn’t it?
And the idea that 4% of controls had the required symptoms of at least moderate severity and at least half the time suggests that the prevalence of a debilitating condition similar to M.E. (even if not as severe as what some people experience) is several times more common than even the highest official prevalence estimates so far have suggested.
ICC and CCC are not picking up people who are merely tired or depressed. Whether everyone who meets those criteria has the same disease that those in the Tahoe epidemic had, I’m not going to venture to say. But people meeting the criteria certainly should be classified as sick, and with something that has a lot in common with classic M.E.
Insofar (as I believe) M.E. is a disease that is at its root one of toxicity, I’m going to suggest from those control figures that it’s not just 500,000 or 1 million or even 2 million Americans who are being affected by that toxicity. The figures cited here make it seem likely to be many many more whose lives are being ruined (even if not quite in the nightmarish way that M.E.ruins lives). And that’s scary.
I don’t know much about how those control groups in the study cited here were chosen though. Unfortunately I wasn’t able to get that journal from Northwestern’s library, which is my usual source.
Maybe it’s like that one study described in Osler’s Web, where people living in a cluster spots chose their own controls from the local area, and then some of those controls later got sick. I’m increasingly convinced from my own research that clusters are still a critically important factor in this disease, and therefore that how the controls are chosen for studies like this is extremely important.
I would feel a lot more reassured about the future of the world – as well as more convinced that CCC/ICC actually are fine for diagnostic purposes – if that I knew that the controls in that study were chosen from the same towns as the cases, therefore. Do you know if that was the case, Cort?
If you read Cort’s next article, on the SolveCFS BioBank, it states that they generally look for family and friends of patients for the controls. So I would think most of these people would tend to be local to the patient though not necessarily so. You should contact the SolveCFS BioBank (Gloria Smith at BioBank@SolveCFS.org or by phone at 704-362-2343) to find out for sure.
Certainly for issues like mold if people are living in the same moldy house members of the same family could have varying levels of symptoms, some qualifying as ME/CFS and some “healthy” even though the healthy patients may have multiple symptoms, just not exercise intolerance or severe cognitive issues.
Thank you, James. That makes things a whole lot clearer in my mind.
Regardless of what people believe about the etiology of this disease, it’s been reported over and over again to run in families – spouses, siblings, and parents/children. It’s also been reported that family members who don’t qualify for an M.E. diagnosis frequently have diseases with similar symptoms (such as fibro or autism).
In addition, if people are close enough friends with someone with M.E. to be willing to participate in a demanding study such as this one, then I would guess that they may have shared specific risk factors – e.g. previously having worked or lived in the same building, at minimum having lived in the same general location. (Paul Levine wrote two papers on the tendency of M.E. clusters to occur in people working in particular buildings, for example. So that is an established risk factor. As are geographic clusters, of course.)
So that being the case, it does not surprise me much at all that 16% of these “healthy controls” would have what we might call “mini-M.E.” and 4% would have out-and-out M.E. It’s almost exactly what I would expect, actually.
Looking at this from one perspective, I am extremely concerned. Cort writes about how a variety of researchers are digging into this biobank data, trying to figure out information about M.E. But if nearly 20% of supposedly healthy controls actually do have at least a precursor condition to M.E., then it may be that their samples will demonstrate some of the same abnormalities as the M.E. patients’ samples. And therefore that important biomakers will be discarded as being irrelevant “because healthy controls had that too.”
Again, it is crazy to have people who meet the ICC defined here as “healthy.” Those people should have been excluded as controls, period.
On the other hand, hearing research that a high percentage of friends and family members of M.E. patients are sick themselves, either with M.E. or very similar but less severe conditions, is one of the more exciting findings that I’ve ever heard about this disease.
What we always have been missing in this disease is basic shoe-leather epidemiology. That’s what solved the puzzle for AIDS – when researchers very early on were able to trace the disease to having had sex with a particular person (or shooting up or getting a blood transfusion), and then looked into what underlying issue may have been responsible.
So if all the “healthy controls” in the Solve ME/CFS biobank are family/friends of patients, then the biobank could be a really important epidemiological resource. Researchers could study those controls over time, to see what percentage of them go on to actually get the disease. And then look at factors that were shared when people do get the disease (mold exposures? Hepatitis B vaccines? something else?), to try to come up with reasonable hypotheses about what could be the cause. And then test those hypotheses.
ICC actually does require PEM (exercise intolerance) as well neurological impairment. 4% of the “healthy controls” had both of those (and a variety of other symptoms) at least moderately severely, at least half the time, Cort reported. Another 12% of healthy controls also had both those symptoms, but less than moderately severely, less than half the time, Cort reported.
If exercise intolerance (at least as defined on the two-day exercise test) is a symptom only seen in M.E. patients, then I’d like to put some of these “healthy controls” on exercise bikes to see how they do. If indeed they do display exercise intolerance in a 2-day test, that would for sure mean that the biobank needs to find some truly healthy controls to give to the researchers that Cort mentioned in his new article, and then to use the family/friends “controls” just to study the disease in an epidemiological way.
I see nothing here that suggests that there is any reason to discard the ICC or CCC. It very well may be correctly identifying people with “pre-M.E.” or “mini-M.E.” in addition to the patients with severe M.E. If so, that would make it potentially extremely useful.
In addition, the idea that many patients who meet the ICC or CCC have psychological issues is no reason at all to consider throwing it out. People with AIDS have dementia and mood issues similar to those of M.E. patients, and no one would suggest that is a reason to define the disease in a different way. Considering the known fact that a variety of pathogens and a variety of toxins can have major effects on mood, the idea that any M.E. patients wouldn’t have psychological issues is what should be surprising.
However, a key issue is to make sure that future research is focused on people who are severely ill with M.E., rather than on people who are only mildly sick. If you’re going to do initial study on a disease like Alzheimer’s, where some people with mild memory issues progress to something horrible and others do not, the way to do it is to learn as much as you can about the people who already have something horrible – the clear cases. And that is what we should be doing here: learning as much as we can about people who already are severely sick with M.E. – the clear cases. And then comparing them to appropriate controls, rather than the inappropriate controls that apparently are currently being used by the biobank.
So again, I’m really really happy to see the issue of severity being brought up in such a forceful way here.
The idea that severity on a very few symptoms should be substituted for the CCC and ICC is something that I think is very premature, however.
Is it possible that a better definition could be written than the ICC or the CCC? Of course. Maybe a simpler definition indeed would do the job just as well. Maybe other symptoms should be added.
However, if anything, the information in this report makes me more convinced than ever that those definitions are pretty good already and that we should think very hard before suggesting that they be thrown out.
The clinicians who wrote the definition have seen patients at many stages of illness and may well have included criteria that – even if it seems unnecessary to diagnose severely ill patients – does a great job of picking out people who are only mildly sick but have the strong potential to become very sick. I don’t think those are the right people to be studying in research right now, but missing them clinically would be extremely unfortunate.
There’s too much that we don’t yet understand about this disease to throw out the observations of specialists who have treated tens of thousands of patients based on a single research study. I have a huge amount of respect for Lenny Jason and his study certainly is interesting, but it’s one more piece of the puzzle, not a reason to start over once again. We’ve come too far already to let that happen.
for me the odd thing about ME – and the thing that distinguishes it from everything else – is that people are worse after activity, Everything else can be found in other disorders.
I am actually appalled by this. I understand that as sufferers we want a better description of our disease, but we have to remember that we do not fully understand the etiology of it!
Without fulling, completely and undeniably understanding the workings of a disease we cannot break down and simplify it! Right now, it is only diagnosed as a matter of exclusion. Anything to explain extreme/severe fatigue and post-exertional malaise being ruled out means it’s CFS/ME.
We are still discovering new etiology of the disease, how are we to simplify it?
My disease is complex, under studied and under funded. Changing the criteria for it to better describe how we feel due to it is not going to help us in anyway! I want treatment, not further slimming- sorry better diagnostic criteria!
The pain I feel in my legs, my bones, my muscles after just going up the stairs surely is much much different to that of non-CFS sufferers.
I believe that we should make the symptomatology more defined rather than broad. Simply cutting down the diagnostic symptoms and creating sub-groups is not going to do much good. This is why it has been denied being changed- we know too little to be able to change the diagnostic criteria completely.
Yes, I want there to be a better understanding of the disease rather than people just thinking it’s just being tired all the time- but I’d rather have tangible treatment rather than hit and miss treatment!
We should fight for better funding to research the disease than something as small as this!
Jason took certified ME/CFS patients and then compared their symptoms to healthy controls. He came with symptoms that zeroed in on the ME/CFS patients. If this early effort or something like it holds up – research studies and clinical will have more real ME/CFS patients in them and should be able to get to heart of ME/CFS better and find better treatments. A good research definition is the foundation for progress elsewhere – that’s why this is a real step forward.
It’s not trying to describe the disease – it’s trying capture the right patients for studies.
Can I sign up as a certified ME /CFS patient?
Something that struck me about the common symptoms that didn’t make the cut in Jason’s statistical analysis, is that I’ve always held that one area where we fall down in talking to researchers, doctors and other people without ME, is language.
I was very physically active before the ME hit me like a truck, and I’ve had a lot of experience of the aches and muscle fatigue involved with working to build up muscle tone, and with general, frequent exercise that pushes at the boundaries of stamina. In my experience, those healthy body sensations are completely separate sensations from the aches and muscle fatigue involved with ME – but there is no difference in the language available for me to use!
Indeed, for one of the sensations that is most characteristic of my experience of ME, there is no word except “ache” available – and yet it isn’t even really an ache in the way I understand that word to properly have meaning; it’s simply that “ache” is the closest I can come in one word. The longer description would be that it’s closer in many ways to “resonation”; it’s like standing next to a loud speaker pumping out heavy bass music (except without sound), like standing in the middle of an earth tremor (but without being shaken), like having all my bones stretched out in tension on a medieval rack (but without actual pain or stretching), like having sung too much crystal (for anyone who’s read Anne McCaffrey’s The Crystal Singer!).
I have a suspicion that if you took ten words from the definitions that both healthy people and people with ME commonly use – and then ask them to define those words/phrases in as much detail as possible, that the results would separate back out into two immediately identifiable groups.
I think one of the problems we have, is that the words we need to describe ME accurately don’t exist, so when we use the next best thing, we end up wrapping back around into the language that health professionals have already recognised as being about healthy bodies and exercise. And I think that’s why we get so many doctors/physiotherapists getting confused and trying to talk to us about “muscle deconditioning” and “building up stamina” when it’s been long proven that ME is not an exercise problem.
…What I don’t know, is whether we can solve that language problem.
I agree! I think that’s why “heavy feeling after exercise “resonated” :)” – it was quite description. I think I know what you mean about that symptoms – . I experienced many times when talking a kind of resonating pain. I hope someone works on developing more accurate and descriptive for the symptom in ME/CFS.
“In my experience, those healthy body sensations are completely separate sensations from the aches and muscle fatigue involved with ME – but there is no difference in the language available for me to use!”
Nicola I agree as well and appreciate the way you’ve articulated this!
For me, prior to ME, muscles after exercise felt “sore” and perhaps a bruise-like sensation. After ME it is much more an “ache” and “stiff” that over time have developed deeper characteristics that defy words. “Ache” and “stiff” certainly feel as inadequate as “fatigue” to describe the reality of ME/CFS.
I know of three massage therapists who say they can feel the difference in muscles. I suppose, given that both feeling and describing difference are subjective, it will be difficult to have these distinctions included in clinical or research definitions. They are certainly part of the reality though!
“In my experience, those healthy body sensations are completely separate sensations from the aches and muscle fatigue involved with ME – but there is no difference in the language available for me to use!”
Nicola I agree as well and appreciate the way you’ve articulated this!
For me, prior to ME, muscles after exercise felt “sore” and perhaps a bruise-like sensation. After ME it is much more an “ache” and “stiff” that over time have developed deeper characteristics that defy words. “Ache” and “stiff” certainly feel as inadequate as “fatigue” to describe the reality of ME/CFS.
I know of three massage therapists who say they can feel the difference in muscles. I suppose, given that both feeling and describing difference are subjective, it will be difficult to have these distinctions included in clinical or research definitions. They are certainly part of the reality though!
Agree about including cranial inflammation however that symptom did not appear for me until several years into the disease when whatever infectious agent? breached the blood brain barrier.
It should be one of the criteria but does not exclude ME/CFS if it has yet to make it’s appearance.
I am interested in what actual symptoms people are experiencing when the term brain inflammation is used. I know there is research evidence pointing to inflammation in the brain, but that seems to me still non-specific, and not in itself a symptom. My symptoms are mental fatigue after mental work, and others such as destractability, not being able to remember what I am doing from moment to moment, which is I think perhaps the same thing as what is referred to as an inability to multitask, but I am not sure.
I also have a question about the heaviness in the legs after exercise. Could someone talk about how much exercise, or what kind of exercise, when it comes on, how long it lasts.
Thanks, Cort, for bringing our attention to this. It is really sobering to think that we have been using a definition that includes so many people in the control group. It really shows how far we are from having an accurate clinical diagnosis. Of course, Lenny’s research was limited to looking at that set of questions. But how do we know any group of people with CFS is a good clean group to look at?
We just have to go by faith that the ME/CFS physicians gave them a representative sample. My guess is that they were probably sicker than the average but hopefully otherwise they fit. They didn’t say how much exercise causes heaviness – all we know is that it was a least moderate heaviness and occurred at least half the time afterwords
Everybody:
What the heck are we talking about “brain inflammation” as a symptom?
If I remember correctly (seldom true) it is pretty recent that there has been any objective information from research seemingly finding such inflammation exists.
I think I learned in school,that the brain does not have internal sensory nerves of the kind that feel localized sensations such as pain. I have a pretty classic case of ME, and it is severe meaning mainly I am housebound, and I have neuro cognitive symptoms, non-refreshing sleep, muscular skeletal pain, fibromyalgia, and “post exertional malaise” which is typically delayed 24 hours. I can walk a little bit but I need a wheel chair to get around in my house.
I would be interested to hear what brain inflammation feels like. No disrespect intended I really just don’t know what this feels like so I cannot identify this in myself.
I am also a bit surprised that “PEM” is not being seen as a core symptom. I have thought that exercise causes immediate symptoms in everyone, but that delayed symptoms are unusual and can be very severe compared to the trigger amount of exercise. It also seems to me that these symptoms are very similar to “sick syndrome” which is just a medical description of immune system activation, which is delayed because it takes some time for the immune system after being triggered to build up to the level that it causes symptoms. We (ME) patients commonly describe this as being like having the flu. Are there really a lot of “ME” patients that don’t have this?
Best wishes to everyone.
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http://www.scientificamerican.com/article/do-the-bacteria-behind-scratch-fever-cause-chronic-fatigue/
“Does the Bacterium behind Cat Scratch Fever Cause Chronic Fatigue?”
New Research on how nanobacteria cause calcification in tissues that prevents antibiotics and other treatments from working. This nanobacteria commonly called Bartonella infection is very hard to detect and can only be detected using advanced methods. There is a newly developed method to overcome this nanobacteria calcification and once that is done treatments become much more effective.
https://www.youtube.com/watch?v=spjzJEME6kI